目的:了解系统性红斑狼疮(SLE)患者外周血单核细胞主要组织相容性复合体(MHC)Ⅰ类链相关分子(MⅠCs)、IL-15表达水平变化及其潜在机制。方法:收集20例SLE患者及20例健康志愿者外周血,分离单核细胞及血清,采用流式细胞术检测单核细胞表面MⅠCs及mIL-15的表达,EILIS法检测血清中干扰素-γ(INF-γ)、干扰素-α(INF-α)浓度,并对单核细胞表面MⅠCs表达水平与血清INF-γ浓度作相关性分析。进一步以SLE患者血清与健康志愿者单核细胞体外孵育,在有或无抗INF-γR存在的情况下,检测单核细胞表面MⅠCs分子的表达情况。结果:SLE患者血清IFN-γ浓度与健康对照组相比有显著性差异,其中IFN-γ在SLE患者为(429.7±145.0)pg/ml[健康对照为(73.8±18.9)pg/ml],二者有显著性差异(P〈0.01);单核细胞MⅠCs及mIL-15的阳性率分别为(37.0±18.1)%和(36.0±7.3)%,而健康志愿者单核细胞MⅠCs及mIL-15的阳性率为(7.2±2.4)%和(7.6±2.5)%。SLE患者MⅠCs及mIL-15阳性率显著高于健康志愿者(P〈0.01);SLE患者单核细胞MⅠCs分子表达水平与血清INF-γ浓度呈正相关;SLE患者血清中高浓度的IFN-γ可以刺激正常人单核细胞表达高水平的MⅠCs及mIL-15。结论:SLE患者血清INF-γ浓度异常升高,导致外周血单核细胞表面MⅠCs及IL-15异常高表达。
Objective: To investigate the surface expression level of MHC class I chain-relate molecules (MICs) and membrane IL-15 on peripheral blood monocytes in patients with system lupus ery- thematosus (SLE). Methods: Twenty patients with SLE and 20 healthy volunteers were included in this study. Peripheral blood monouclear cells (PBMCs) were harvested by density gradient centrifugation, and M ICs and IL-15 on monocytes were detected by flow cytometry. Serum con- centration of IFN-γ were examined by ELISA. The relationship between monocyte MICs and se- rum IFN-γ were analyzed. Purified monocytes from healthy donors were incubated with sera from SLE patients in the presence or absence of blocked anti-INF-TR antibodies, and the MICs expression on monocytes were further studied. Results: The concentration of IFN-γ in SLE patients (150.3-669.5 pg/ml, [-429. 7±145. 01 pg/ml) was significantly higher than in normal controls (18.8-88.2 pg/ml, [-73.8±18.91 pg/ml). The expression of MICs on monocytes was (7.2±2.4)% in normal controls versus (37.0±18.1)% in SLE patients, mIL-15 expression of CD14+ monoeytes in SLE patients was (36.0±7.3)%, which is significantly higher than those in normal controls ([7. 6± 2. 5]%). The concentration of IFN-γ in patients was significantly correlated with the expression of M[Cs on monocytes. Sera from SLE patients can promote the expression of MICs and mIL-15 on monocytes, but this effects can be prevented in the condition of IFN-γ blocking. Conclusion: Increased sera IFN-γ in patients with SLE is responsible for the aberrant expression of MICs and mIL-15 on monocytes.